Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis

Camille Jardeleza, Dijana Miljkovic, Leonie Baker, Samuel Boase, Neil Cheng Wen Tan, Simon A. Koblar, Peter Zalewski, Maureen Rischmueller, Susan Lester, Amanda Drilling, Damien Jones, Lor Wai Tan, Peter John Wormald, Sarah Vreugde

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: The role of inflammasomes in chronic inflammation has been the subject of intense research in recent years. Chronic rhinosinusitis (CRS), a persistent inflammatory disease, continues to be investigated hoping that a clearer pathophysiologic description will guide discovery of future treatment modalities. This study investigates the role of inflammasome complexes in CRS patients with Staphylococcus aureus biolm infection, a key culprit associated with disease severity and recalcitrance. Methodology: Sinonasal tissue samples were collected from CRS patients with (P+) and without (P-) polyps and controls. S. aureus biolm status was obtained using fluorescence in situ hybridization and classied as biolm positive (B+) or negative (B-). RNA was analysed using a Human Inflammasome PCR array, proling the expression of 84 genes involved in inflammasome function. Results: Sixteen samples were obtained: 5 B+P+, 5 B-P-and 6 controls. Comparing B+P+ vs. controls showed the greatest number of differentially expressed genes. In particular, Absent in Melanoma 2 (AIM2) was consistently and signicantly up-regulated in the B+P+ vs. B-P-and controls. In contrast, when comparing the B-P-vs. controls, no genes showed signicant changes. Conclusion: Our results indicate the involvement of inflammasome complexes and their signalling pathways in CRS patients with polyps and S. aureus biolms. In particular, AIM2, activated by intracellular double-stranded DNA, is up-regulated in this group, implying that S. aureus may play a role in intracellular triggering of the inflammasome response. Studies with further patient stratification and assessing corresponding protein expression are needed to further characterize the role of inflammasomes in CRS.

LanguageEnglish
Pages315-322
Number of pages8
JournalRhinology
Volume51
Issue number4
DOIs
Publication statusPublished - 2013

Keywords

  • Absent in melanoma 2
  • AIM2
  • Biolms
  • Chronic rhinosinusitis
  • CRS
  • Inflammasome
  • Innate immunity
  • S. aureus
  • Staphylococcus aureus

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Jardeleza, C., Miljkovic, D., Baker, L., Boase, S., Tan, N. C. W., Koblar, S. A., ... Vreugde, S. (2013). Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis. Rhinology, 51(4), 315-322. https://doi.org/10.4193/Rhino13.045
Jardeleza, Camille ; Miljkovic, Dijana ; Baker, Leonie ; Boase, Samuel ; Tan, Neil Cheng Wen ; Koblar, Simon A. ; Zalewski, Peter ; Rischmueller, Maureen ; Lester, Susan ; Drilling, Amanda ; Jones, Damien ; Tan, Lor Wai ; Wormald, Peter John ; Vreugde, Sarah. / Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis. In: Rhinology. 2013 ; Vol. 51, No. 4. pp. 315-322.
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abstract = "Background: The role of inflammasomes in chronic inflammation has been the subject of intense research in recent years. Chronic rhinosinusitis (CRS), a persistent inflammatory disease, continues to be investigated hoping that a clearer pathophysiologic description will guide discovery of future treatment modalities. This study investigates the role of inflammasome complexes in CRS patients with Staphylococcus aureus biolm infection, a key culprit associated with disease severity and recalcitrance. Methodology: Sinonasal tissue samples were collected from CRS patients with (P+) and without (P-) polyps and controls. S. aureus biolm status was obtained using fluorescence in situ hybridization and classied as biolm positive (B+) or negative (B-). RNA was analysed using a Human Inflammasome PCR array, proling the expression of 84 genes involved in inflammasome function. Results: Sixteen samples were obtained: 5 B+P+, 5 B-P-and 6 controls. Comparing B+P+ vs. controls showed the greatest number of differentially expressed genes. In particular, Absent in Melanoma 2 (AIM2) was consistently and signicantly up-regulated in the B+P+ vs. B-P-and controls. In contrast, when comparing the B-P-vs. controls, no genes showed signicant changes. Conclusion: Our results indicate the involvement of inflammasome complexes and their signalling pathways in CRS patients with polyps and S. aureus biolms. In particular, AIM2, activated by intracellular double-stranded DNA, is up-regulated in this group, implying that S. aureus may play a role in intracellular triggering of the inflammasome response. Studies with further patient stratification and assessing corresponding protein expression are needed to further characterize the role of inflammasomes in CRS.",
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author = "Camille Jardeleza and Dijana Miljkovic and Leonie Baker and Samuel Boase and Tan, {Neil Cheng Wen} and Koblar, {Simon A.} and Peter Zalewski and Maureen Rischmueller and Susan Lester and Amanda Drilling and Damien Jones and Tan, {Lor Wai} and Wormald, {Peter John} and Sarah Vreugde",
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Jardeleza, C, Miljkovic, D, Baker, L, Boase, S, Tan, NCW, Koblar, SA, Zalewski, P, Rischmueller, M, Lester, S, Drilling, A, Jones, D, Tan, LW, Wormald, PJ & Vreugde, S 2013, 'Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis', Rhinology, vol. 51, no. 4, pp. 315-322. https://doi.org/10.4193/Rhino13.045

Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis. / Jardeleza, Camille; Miljkovic, Dijana; Baker, Leonie; Boase, Samuel; Tan, Neil Cheng Wen; Koblar, Simon A.; Zalewski, Peter; Rischmueller, Maureen; Lester, Susan; Drilling, Amanda; Jones, Damien; Tan, Lor Wai; Wormald, Peter John; Vreugde, Sarah.

In: Rhinology, Vol. 51, No. 4, 2013, p. 315-322.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inflammasome gene expression alterations in Staphylococcus aureus biofilm-associated chronic rhinosinusitis

AU - Jardeleza, Camille

AU - Miljkovic, Dijana

AU - Baker, Leonie

AU - Boase, Samuel

AU - Tan, Neil Cheng Wen

AU - Koblar, Simon A.

AU - Zalewski, Peter

AU - Rischmueller, Maureen

AU - Lester, Susan

AU - Drilling, Amanda

AU - Jones, Damien

AU - Tan, Lor Wai

AU - Wormald, Peter John

AU - Vreugde, Sarah

PY - 2013

Y1 - 2013

N2 - Background: The role of inflammasomes in chronic inflammation has been the subject of intense research in recent years. Chronic rhinosinusitis (CRS), a persistent inflammatory disease, continues to be investigated hoping that a clearer pathophysiologic description will guide discovery of future treatment modalities. This study investigates the role of inflammasome complexes in CRS patients with Staphylococcus aureus biolm infection, a key culprit associated with disease severity and recalcitrance. Methodology: Sinonasal tissue samples were collected from CRS patients with (P+) and without (P-) polyps and controls. S. aureus biolm status was obtained using fluorescence in situ hybridization and classied as biolm positive (B+) or negative (B-). RNA was analysed using a Human Inflammasome PCR array, proling the expression of 84 genes involved in inflammasome function. Results: Sixteen samples were obtained: 5 B+P+, 5 B-P-and 6 controls. Comparing B+P+ vs. controls showed the greatest number of differentially expressed genes. In particular, Absent in Melanoma 2 (AIM2) was consistently and signicantly up-regulated in the B+P+ vs. B-P-and controls. In contrast, when comparing the B-P-vs. controls, no genes showed signicant changes. Conclusion: Our results indicate the involvement of inflammasome complexes and their signalling pathways in CRS patients with polyps and S. aureus biolms. In particular, AIM2, activated by intracellular double-stranded DNA, is up-regulated in this group, implying that S. aureus may play a role in intracellular triggering of the inflammasome response. Studies with further patient stratification and assessing corresponding protein expression are needed to further characterize the role of inflammasomes in CRS.

AB - Background: The role of inflammasomes in chronic inflammation has been the subject of intense research in recent years. Chronic rhinosinusitis (CRS), a persistent inflammatory disease, continues to be investigated hoping that a clearer pathophysiologic description will guide discovery of future treatment modalities. This study investigates the role of inflammasome complexes in CRS patients with Staphylococcus aureus biolm infection, a key culprit associated with disease severity and recalcitrance. Methodology: Sinonasal tissue samples were collected from CRS patients with (P+) and without (P-) polyps and controls. S. aureus biolm status was obtained using fluorescence in situ hybridization and classied as biolm positive (B+) or negative (B-). RNA was analysed using a Human Inflammasome PCR array, proling the expression of 84 genes involved in inflammasome function. Results: Sixteen samples were obtained: 5 B+P+, 5 B-P-and 6 controls. Comparing B+P+ vs. controls showed the greatest number of differentially expressed genes. In particular, Absent in Melanoma 2 (AIM2) was consistently and signicantly up-regulated in the B+P+ vs. B-P-and controls. In contrast, when comparing the B-P-vs. controls, no genes showed signicant changes. Conclusion: Our results indicate the involvement of inflammasome complexes and their signalling pathways in CRS patients with polyps and S. aureus biolms. In particular, AIM2, activated by intracellular double-stranded DNA, is up-regulated in this group, implying that S. aureus may play a role in intracellular triggering of the inflammasome response. Studies with further patient stratification and assessing corresponding protein expression are needed to further characterize the role of inflammasomes in CRS.

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KW - AIM2

KW - Biolms

KW - Chronic rhinosinusitis

KW - CRS

KW - Inflammasome

KW - Innate immunity

KW - S. aureus

KW - Staphylococcus aureus

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U2 - 10.4193/Rhino13.045

DO - 10.4193/Rhino13.045

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